ArticleGenetics2013
Gene copy-number variation in haploid and diploid strains of the yeast Saccharomyces cerevisiae.
Article in Genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed.
- From Oak to Wine: Evolution, Admixture, and Adaptation of California and British Columbia Saccharomyces Cerevisiae Wine Strains.Genome biology and evolution · 2026Article
- High-throughput mapping of spontaneous mitotic crossover and genome instability events with sci-L3-Strand-seq.Nucleic acids research · 2026Article
- Article
- Formation of chromosomal rearrangements inbioRxiv : the preprint server for biology · 2025Article
- Comprehensive Genomic Analysis ofGenes · 2025Article
- Template switching during DNA replication is a prevalent source of adaptive gene amplification.eLife · 2025Article
- Comparative Proteomics of Two Flor Yeasts in Sparkling Wine Fermentation: First Approach.Foods (Basel, Switzerland) · 2025Article
- Template switching during DNA replication is a prevalent source of adaptive gene amplification.bioRxiv : the preprint server for biology · 2024Article
- Genomic and metabolic instability during long-term fermentation of an industrialFrontiers in bioengineering and biotechnology · 2024Article
- Tandem gene duplications contributed to high-level azole resistance in a rapidly expanding Candida tropicalis population.Nature communications · 2023Article
- The Dynamic Fungal Genome: Polyploidy, Aneuploidy and Copy Number Variation in Response to Stress.Annual review of microbiology · 2023Review
- Whole genome sequencing of Canadian Saccharomyces cerevisiae strains isolated from spontaneous wine fermentations reveals a new Pacific West Coast Wine clade.G3 (Bethesda, Md.) · 2023Article
- Delineation of two multi-invasion-induced rearrangement pathways that differently affect genome stability.Genes & development · 2023Article
- Identifying Targets of Selection in Laboratory Evolution Experiments.Journal of molecular evolution · 2023Review
- Hotspot of de novo telomere addition stabilizes linear amplicons in yeast grown in sulfate-limiting conditions.Genetics · 2023Article
- Delineation of two multi-invasion-induced rearrangement pathways that differently affect genome stability.bioRxiv : the preprint server for biology · 2023Article
- Neural networks enable efficient and accurate simulation-based inference of evolutionary parameters from adaptation dynamics.PLoS biology · 2022Article
- Article
- Bursts of Genomic Instability Potentiate Phenotypic and Genomic Diversification inFrontiers in genetics · 2022Article
- DNA Repair in Haploid Context.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The increasing ability to sequence and compare multiple individual genomes within a species has highlighted the fact that copy-number variation (CNV) is a substantial and underappreciated source of genetic diversity. Chromosome-scale mutations occur at rates orders of magnitude higher than base substitutions, yet our understanding of the mechanisms leading to CNVs has been lagging. We examined CNV in a region of chromosome 5 (chr5) in haploid and diploid strains of Saccharomyces cerevisiae. We optimized a CNV detection assay based on a reporter cassette containing the SFA1 and CUP1 genes that confer gene dosage-dependent tolerance to formaldehyde and copper, respectively. This optimized reporter allowed the selection of low-order gene amplification events, going from one copy to two copies in haploids and from two to three copies in diploids. In haploid strains, most events involved tandem segmental duplications mediated by nonallelic homologous recombination between flanking direct repeats, primarily Ty1 elements. In diploids, most events involved the formation of a recurrent nonreciprocal translocation between a chr5 Ty1 element and another Ty1 repeat on chr13. In addition to amplification events, a subset of clones displaying elevated resistance to formaldehyde had point mutations within the SFA1 coding sequence. These mutations were all dominant and are proposed to result in hyperactive forms of the formaldehyde dehydrogenase enzyme.
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